摘要
目的 :探讨Ⅳ型胶原酶 (MMP2 及MMP9)在糖尿病大鼠肺组织表达的变化及蛋白激酶C(PKC)的作用。方法 :STZ腹腔注射制作糖尿病大鼠模型 ,4周后观察肺组织的病理改变 ,免疫组化方法检测MMP2 及MMP9在糖尿病大鼠肺组织表达的变化 ,采用改良的Takay法测定PKC活性 ,蛋白质免疫印迹分析 (Western -blot)及免疫组化方法检测TGF - β1表达含量的变化。结果 :DM大鼠 4周后肺泡间隔及毛细血管壁增厚 ,肺间质胶原成分增多 ,肺组织PKC活性增强 ,TGF - β1表达增多 ,MMP2 及MMP9表达下降。结论 :在糖尿病大鼠肺组织高糖环境下 ,PKC被激活导致TGF - β1表达增高 ,MMP2 、MMP9表达下降 ,引起细胞外基质 (ECM )合成降解失调 ,可能参与了糖尿病肺部并发症的发生及发展。
Objective:To observe the pathologic changes,and to investigate the alteration of PKC ?MMP 2?MMP 9 in pulmonary tissues in diabetic rats.Methods:Diabetic model rats were induced by intraperitoneally injected streptozotozin (STZ). After 4 weeks, we observed the pathologic changes in lungs, tested protein kinase C (PKC) activities by isotope in lungs of model rats, tested transforming growth factor (TGF-β 1) by Western blotting and immunohistochemical analysis, determined the expression of MMP 2?MMP 9 using immunohistochemical analysis.Results:After STZ administration for 4 weeks, we observed thickened pulmonary capillary basal lamina and increasing number of fibres in DM rats. The activities of PKC and TGF-β 1 levels were found increased, at the mean time, the expression of MMP 2?MMP 9 decreased.Conclusions: Hyperglycemia -DAG-PKC signal pathways might play an important role in the increased activities of TGF-β 1 and the decreased expression of MMP 2?MMP 9 , which induced the imbalance of ECM might play an important role in diabetic lung.
出处
《中国现代医学杂志》
CAS
CSCD
2003年第18期24-28,共5页
China Journal of Modern Medicine